<![CDATA[Merokok dan paparan produk tembakau modern merupakan faktor risiko utama berbagai penyakit kronis melalui aktivasi stres oksidatif dan inflamasi sistemik. Asap rokok mengandung ribuan senyawa toksik yang meningkatkan pembentukan reactive oxygen species (ROS), menyebabkan disfungsi mitokondria, serta mengaktivasi jalur inflamasi seperti nuclear factor-kappa B (NF-κB) dan inflammasom NLRP3. Aktivasi jalur tersebut meningkatkan produksi sitokin proinflamasi, memperkuat kerusakan jaringan, dan mempertahankan inflamasi kronis derajat rendah. Bukti terkini menunjukkan bahwa rokok konvensional maupun rokok elektronik berkontribusi terhadap peningkatan stres oksidatif, penurunan bioavailabilitas nitric oxide, aktivasi molekul adhesi endotel, serta disfungsi vaskular yang berperan dalam aterosklerosis. Interaksi antara stres oksidatif dan inflamasi membentuk suatu aksis patofisiologis yang menjadi mekanisme sentral perkembangan berbagai penyakit terkait rokok, termasuk penyakit paru obstruktif kronik, penyakit kardiovaskular, gangguan metabolik, dan penyakit neurodegeneratif. Literature review ini bertujuan menguraikan secara sistematis peran aksis stres oksidatif–inflamasi dalam patogenesis penyakit terkait rokok, termasuk dampak produk tembakau generasi baru serta implikasi klinis dan potensi strategi terapeutiknya. Penelitian menggunakan desain literature review berdasarkan pedoman PRISMA 2020 dengan sumber data dari Scopus, PubMed, ScienceDirect, dan Google Scholar. Sebanyak 18 artikel yang diterbitkan pada tahun 2020–2026 dan memenuhi kriteria inklusi dianalisis. Hasil menunjukkan bahwa paparan asap rokok dan aerosol produk tembakau generasi baru mengaktivasi aksis stres oksidatif–inflamasi melalui peningkatan ROS, aktivasi NF-κB, inflammasom NLRP3, dan pyroptosis yang berdampak pada disfungsi endotel, aterosklerosis, gangguan metabolik, serta peningkatan biomarker inflamasi. Disimpulkan bahwa aksis stres oksidatif–inflamasi merupakan mekanisme utama yang menghubungkan paparan rokok dengan berbagai penyakit kronis. Smoking and exposure to modern tobacco products remain major risk factors for various chronic diseases through the activation of oxidative stress and systemic inflammation. Cigarette smoke contains thousands of toxic compounds that increase the production of reactive oxygen species (ROS), induce mitochondrial dysfunction, and activate inflammatory pathways such as nuclear factor-kappa B (NF-κB) and the NLRP3 inflammasome. Activation of these pathways enhances the production of pro-inflammatory cytokines, exacerbates tissue damage, and sustains chronic low-grade inflammation. Recent evidence indicates that both conventional cigarettes and electronic cigarettes contribute to increased oxidative stress, reduced nitric oxide bioavailability, activation of endothelial adhesion molecules, and vascular dysfunction involved in the development of atherosclerosis. The interaction between oxidative stress and inflammation forms a pathophysiological axis that serves as a central mechanism in the progression of smoking-related diseases, including chronic obstructive pulmonary disease, cardiovascular diseases, metabolic disorders, and neurodegenerative diseases. This literature review aimed to systematically examine the role of the oxidative stress–inflammation axis in the pathogenesis of smoking-related diseases, including the impact of next-generation tobacco products, as well as their clinical implications and potential therapeutic strategies. The study employed a literature review design based on the PRISMA 2020 guidelines, using data sources from Scopus, PubMed, ScienceDirect, and Google Scholar. A total of 18 articles published between 2020 and 2026 that met the inclusion criteria were analysed. The findings indicate that exposure to cigarette smoke and aerosols from next-generation tobacco products activates the oxidative stress–inflammation axis through increased ROS production, NF-κB activation, NLRP3 inflammasome activation, and pyroptosis, resulting in endothelial dysfunction, atherosclerosis, metabolic disturbances, and elevated inflammatory biomarkers. In conclusion, the oxidative stress–inflammation axis represents a key mechanism linking tobacco exposure to various chronic diseases.]]>
